Nitric oxide production in murine leishmaniasis: Correlation of progressive infection with increasing systemic synthesis of nitric oxide
Nitric oxide production in murine leishmaniasis: Correlation of progressive infection with increasing systemic synthesis of nitric oxide
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DOI：
10.4269/ajtmh.1996.54.486
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发表时间：
1996-05-01
影响因子：
3.3
通讯作者：
Hibbs, JB
中科院分区：
文献类型：
--
作者：
Evans, TG;Reed, SS;Hibbs, JB
先前的研究表明，在BALB/c和C3H小鼠模型中，一氧化氮（NO）的产生是控制利什曼原虫感染的主要效应机制。小鼠的易感性与感染后内在NO的产生有关。我们之前已经表明，口服N-(ω)-单甲基- l-精氨酸阻断全身NO生成导致NO减少和感染加剧。C3H小鼠在初始感染后不久也明显比BALB/c小鼠合成更多的NO。我们现在表明，在感染后期，随着病变大小的增加，BALB/c NO的产生实际上超过了C3H感染的治愈阶段。此外，用氨铵甲氨胺治疗可以改善但不能治愈BALB/c小鼠，但可以减少全身寄生虫负荷，同时减少NO的产生。这些结果表明，体内系统测量的NO水平在某些情况下可能反映了正在进行的寄生负荷，并且NO的产生并不总是与治疗反应相关。
Previous studies have shown that nitric oxide (NO) production is a major effector mechanism in the control of Leishmania major infection in the BALB/c and C3H murine models. The susceptibility of mice correlates with intrinsic NO production after infection. We have previously shown that blocking of systemic NO production with oral N-(omega)-monomethyl-L-arginine results in decreased NO and exacerbated infection. The C3H mice also synthesize markedly more NO than BALB/c mice shortly after initial infection. We now show that late in infection, as the lesion size is increasing, the BALB/c NO production actually exceeds that seen during the curative stages of the C3H infection. In addition, treatnent with meglumine antimoniate, which ameliorates but does not cure the BALB/c mouse, results in decreased systemic parasite load with a concomitant decrease in NO production. These results imply that in vivo, systemically measured levels of NO may in some circumstances reflect ongoing parasitic load, and that NO production is not always correlated with a curative response.